Deposition in brain

In the rare hereditary disease essential pentosuria, considerable quantities of L-xylulose appear in the urine because of absence of the enzyme necessary to reduce L-xylulose to xyhtol. Parenteral administration of xylitol may lead to oxalosis, involving calcium oxalate deposition in brain and kidneys (Figure 20-4). Various drugs markedly increase the rate at which glucose enters the... 

Bilirubin is a product of the breakdown of haemoglobin in red blood cells. Neonatal jaundice occurs when bilirubin builds up faster than a newborn baby s liver is able to break it down. This results in the deposition of water-insoluble bilirubin in the skin (giving the skin a yellow colour) and untreated it can lead to damage of the central nervous system by deposition in brain cells. 

Willem M, Dewachter I, Smyth N, Van Dooren T, Borghgraef P, Haass C, Van Leuven F (2004) beta-site amyloid precursor protein cleaving enzyme 1 increases amyloid deposition in brain parenchyma but reduces cerebrovascular amyloid angiopathy in aging BACE x APP[V717I] double-transgenic mice. Am J Pathol 165 1621-1631. 

Bacskai BJ, Kajdasz ST, Christie RH, Carter C, Games D, Seubert P et al (2001) Imaging of amyloid-beta deposits in brains of living mice permits direct observation of clearance... 

Qu BX, Xiang Q, Li L, Johnston SA, Hynan LS, Rosenberg RN et al (2007) Abeta42 gene vaccine prevents Abeta42 deposition in brain of double transgenic mice. J Neurol Sci 260 204-213... 

Amyloid Precursor Protein (APP) derived amyloid peptide (Abeta) depositions in brains of Alzheimer s syndrome (AD) -patients preferentially consist of N-terminal modified pyroglutamyl (pGlu) Abeta in... 

Toxicity. The toxicity of barium compounds depends on solubility (47—49). The free ion is readily absorbed from the lung and gastrointestinal tract. The mammalian intestinal mucosa is highly permeable to Ba " ions and is involved in the rapid flow of soluble barium salts into the blood. Barium is also deposited in the muscles where it remains for the first 30 h and then is slowly removed from the site (50). Very Httle is retained by the fiver, kidneys, or spleen and practically none by the brain, heart, and hair. 

Acute phase reactants (e.g., C-reactive protein) are proteins that increase during inflammation and are deposited in damaged tissues. They were first discovered in the serum, but are now known to be involved in inflammatory processes in the brain (e.g., found in the brain of Alzheimer patients and associated with amyloid plaques). 

The identification, using analytical microprobe and solid-state magic-angle nuclear magnetic resonance (NM techniques, of aluminosilicate deposits in the cores of the pathognomic senile plaques in the brains of Alzheimer subjects (Candy et al., 1986) has prompted widespread scientific and public concern, and controversy with regard to the possible aetiological role of environmental aluminium and aluminosilicates in senile dementia (Walton, 1991). 

The Leggett Model simulates the age-dependence of lead kinetics on such factors as bone turnover rates, partitioning between soft tissues and excreta, removal half-times in liver, kidneys, and red blood cells, and the deposition fraction in brain. The model structure represents a compromise between biological realism and practical considerations regarding the quantity and quality of information available to determine parameter values (Leggett 1993). 

Antibodies raised against the Ap peptide were subsequently used to identify more diffuse types of Ap-containing deposits in AD brain by immunohistochemistry. Diffuse Ap peptide deposits lack the... 

Adults require 1-2 mg of copper per day, and eliminate excess copper in bile and feces. Most plasma copper is present in ceruloplasmin. In Wilson s disease, the diminished availability of ceruloplasmin interferes with the function of enzymes that rely on ceruloplasmin as a copper donor (e.g. cytochrome oxidase, tyrosinase and superoxide dismutase). In addition, loss of copper-binding capacity in the serum leads to copper deposition in liver, brain and other organs, resulting in tissue damage. The mechanisms of toxicity are not fully understood, but may involve the formation of hydroxyl radicals via the Fenton reaction, which, in turn initiates a cascade of cellular cytotoxic events, including mitochondrial dysfunction, lipid peroxidation, disruption of calcium ion homeostasis, and cell death. 

Borchelt, D. R., Ratovitski, T., Van Lare, J. et al. Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins. Neuron 19 939-945,1997. 

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